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Oedema Secondary (oedema + secondary)

Distribution by Scientific Domains
Medical Sciences100%

Kinds of Oedema Secondary

  • macular oedema secondary
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    Selected Abstracts

    Intravitreal anti-vascular endothelial growth factor therapy with bevacizumab for tuberous sclerosis with macular oedema

    ACTA OPHTHALMOLOGICA, Issue 3 2010
    Wataru Saito
    Abstract. Purpose:, To describe two patients with macular oedema secondary to tuberous sclerosis complex (TSC) who were treated with intravitreal bevacizumab injection. Methods:, Interventional case reports. Bevacizumab 1.25 mg was injected into the vitreous of two patients with TSC-associated macular oedema / exudative retinal detachment. Vascular endothelial growth factor (VEGF) concentration in the vitreous fluid was measured by enzyme-linked immunosorbent assay (ELISA) in one of these patients. Results:, Patient 1: a 22-year-old woman with TSC was diagnosed as having multiple retinal hamartomas in both eyes. Eleven years later, the patient developed macular oedema with epiretinal membrane formation in the right eye. The patient underwent pars-plana vitrectomy with retinal photocoagulation for retinal tumours. VEGF concentration in the vitreous fluid was high compared to that in patients without retinal vascular diseases. Recurrent macular oedema disappeared by intravitreal injection of bevacizumab. Patient 2: a 32-year-old woman with TSC-associated retinal hamartoma, temporally showing macular exudative retinal detachment, developed neovascularization originated from the tumour. By intravitreal bevacizumab injection, the tumour size reduced markedly with regression of neovascularization. Conclusion:, These results suggest that VEGF derived from retinal hamartomas causes macular oedema associated with TSC. Intravitreal injections of bevacizumab may be a useful therapeutic option for macular oedema secondary to TSC. [source]

    Retinal artery occlusion following intravitreal anti-VEGF therapy

    ACTA OPHTHALMOLOGICA, Issue 2 2010
    Therese Von Hanno
    Abstract. Purpose:, Anti-vascular endothelial growth factor (anti-VEGF) therapy effectively inhibits angiogenesis and is now enjoying widespread use in the treatment of age-related macular degeneration (AMD). It may also have a role in the treatment of macular oedema secondary to other conditions. VEGF is a signalling molecule that has a variety of roles, including vasoregulation and effects on the coagulation homeostasis. Anti-VEGF therapy may therefore have adverse effects on ocular blood flow. Methods:, Two cases of retinal artery occlusion after intravitreal injection of anti-VEGF are presented. Both patients were given the treatment to reduce macular oedema secondary to central retinal vein occlusion. Possible mechanisms are discussed. Results:, Patient 1 developed a central retinal artery occlusion within 1 month of an intravitreal injection of ranibizumab (Lucentis®). The macular oedema was totally resolved at 1 month; final visual acuity (VA) was light perception. Patient 2 developed a branch retinal artery occlusion in the macula 2 days after an intravitreal injection of bevacizumab (Avastin®). The macular oedema was almost resolved within 1 week and did not recur; final VA was 0.6. Conclusions:, Anti-VEGF therapy may have a role in the treatment of macular oedema caused by central retinal vein occlusions. However, our report indicates that the therapeutic principle may be associated with an increased risk of retinal arterial occlusions. [source]

    Changes of aqueous vascular endothelial growth factor and pigment epithelium-derived factor following intravitreal bevacizumab for macular oedema secondary to branch retinal vein occlusion

    CLINICAL & EXPERIMENTAL OPHTHALMOLOGY, Issue 5 2009
    Sung P Park MD
    Abstract Background:, To investigate sequential changes of aqueous vascular endothelial growth factor (VEGF) and pigment epithelium-derived factor (PEDF) in macular oedema secondary to branch retinal vein occlusion (BRVO) following intravitreal injection of bevacizumab (IVB). Methods:, We recruited 10 healthy controls and 40 patients with BRVO. Aqueous levels of VEGF and PEDF were measured by ELISA at the time of IVB and 6 weeks later. Non-response to IVB was defined as showing persistent macular oedema based on reduction of central macular thickness by less than 20% from baseline measurements by optical coherence tomography and vision improvement by <0.3 logMAR at 6 weeks after IVB. Fluorescein angiography was performed after resolution of foveal haemorrhage. We compared aqueous levels of VEGF and PEDF between responders and non-responders. Results:, The aqueous levels of VEGF and PEDF were significantly higher in 16 non-responders than in 24 responders at baseline measurements (491 ± 231 pg/mL vs. 250 ± 112 pg/mL, P < 0.001; 32 ± 4 ng/mL vs. 25 ± 5 ng/mL, P < 0.001, respectively). Six weeks after IVB, the aqueous levels of VEGF and PEDF were still higher in non-responders than in responders (388 ± 141 pg/mL vs. 104 ± 40 pg/mL, P < 0.001; 30 ± 8 ng/mL vs. 18 ± 5 ng/mL, P < 0.001, respectively). Fluorescein angiography revealed that non-responders showed higher frequencies of macular ischaemia and ischaemic BRVO. Conclusions:, Our results indicate that aqueous VEGF levels are associated with persistent macular oedema secondary to ischaemic BRVO following IVB. [source]